Pathology of COVID-19 across different tissues

In a recent study published in cellresearchers investigated the pathophysiology of coronavirus disease 2019 (COVID-19) in multiple tissues, including lungs, kidneys, heart and brain, to better understand acute and long-term symptoms.

Background

coronavirus (CoVs), including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), typically infect the respiratory and gastrointestinal tracts of the host species. However, pathological studies have confirmed that SARS-CoV-2 infection clinically manifests in multiple organs. The degree of involvement of different organs may be reliable markers of adverse COVID-19 outcomes and PASC. PASC, or symptomatic COVID-19 that has been ongoing for more than 12 weeks, can affect the host’s lungs, kidneys, heart, and brain with varying degrees of severity.

About research

In the present study, researchers performed a thorough cross-sectional analysis of clinical and pathological data of COVID-19 cases from the initial pandemic peak. Additionally, they evaluated this data for the presence of Alzheimer’s disease (AD) neuropathology. They selected 9 of his 15 COVID-19 autopsies for study analysis, which was conducted from April 17 to June 4, 2020. Five of his remaining had non-COVID-19 brains, three of which were her AD cases.

Two forensic physicians, a geriatrician, and a neurologist reviewed the medical charts of all nine study participants retrospectively. They clinically checked for the presence of comorbidities, dementia, delirium, and sepsis. The team collected tissue samples from corpses infected with SARS-CoV-2 for pathological examination.

This included one section per lung lobe, five heart sections from the central horizontal slice, and one section from each kidney including cortex and medulla. They also took seven slices of his brain from the frontal, temporal, parietal, and occipital lobes. Hippocampus – entorhinal cortex. pons; and cerebellum. The team also performed routine histological examination of these sections using the hematoxylin-eosin (H&E) staining technique.

In addition, researchers quantified SARS-CoV-2 ribonucleic acid (RNA) load in these tissues via quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and droplet digital PCR (ddPCR). did. Finally, researchers checked inflammatory infiltrates and microthrombi in the left lower lung lobe, right kidney, left ventricle, frontal lobe of the forebrain, and pons of the hindbrain for the presence of SARS-CoV-2. Due to the small number of cases, the team used nonparametric statistical tests and the Friedman test to compare different tissues of subjects. They used Mann-Whitney’s U test to compare score differences between cases and controls for each organ.

Survey results

The main finding was that it is the most likely cause of PASC rather than persistent inflammation and persistent SARS-CoV-2 replication. Inflammatory and immune-mediated changes potentiate the direct cytopathic damage caused by SARS-CoV-2. These highlight epithelial and endothelial damage, vascular leakage, and attenuation of T-cell responses, along with hyperactivation of macrophage-lineage cells. Therefore, multiple organs are involved. In some cases, lung failure causes severe hypoxia in all tissues.

The authors found that the organ with the highest SARS-CoV-2 antigen burden was the lungs, with the kidneys sharing the burden, albeit to a lesser extent. However, there were rare endothelial cells or pontine neurons in the heart and brain, and there was no evidence of active SARS-CoV-2 replication. , with significantly more microthrombosis and abundant T lymphocytes.

Furthermore, they observed that the heart had rare T lymphocytes, minimal SARS-CoV-2 traces in the endothelium-endocardium, and foci of activated macrophages. The brain similarly showed minimal traces of SARS-CoV-2 and rare T-lymphocytes, but prominent frontal cortical lesions that appear to be related to pre-existing neurodegeneration due to AD but not COVID-19. demonstrated microglial activation. On the contrary, pons showed the highest microglial activation associated with SARS-CoV-2 infection.

Conclusion

The current study has provided a remarkable pathological picture of how SARS-CoV-2 invades various human tissues. We have shown that lung and kidney tissue damage may be directly attributed to SARS-CoV-2-induced cytopathic effects and subsequent inflammation-mediated mechanisms. but,

Damage to the heart and brain from COVID-19 was primarily due to abnormal and persistent inflammation. Therefore, to fully recover from COVID-19, you will need to end both, which can take many months.

A better understanding of the short- and long-term adverse effects of COVID-19 could help improve care for COVID-19 patients, especially after the acute phase of the disease. For example, some patients may preferentially require physical and cognitive training and psychosocial support during recovery to restore previous function.